Zobrazeno 1 - 10
of 14
pro vyhledávání: '"Hansell A"'
Publikováno v:
Upsala Journal of Medical Sciences
Objectives. Accumulation of extracellular matrix (ECM) components is an early sign of diabetic nephropathy. Also the glycosaminoglycan hyaluronan (HA) is elevated in the renal interstitium during experimental diabetes. The mammalian target of rapamyc
Autor:
Angelica Fasching, Fredrik Palm, Peter Hansell, Masaomi Nangaku, Malou Friederich-Persson, Stephanie Franzén
Publikováno v:
American Journal of Physiology-Renal Physiology. 306:F1171-F1178
One-third of diabetes mellitus patients develop diabetic nephropathy, and with underlying mechanisms unknown it is imperative that diabetic animal models resemble human disease. The present study investigated the susceptibility to develop diabetic ne
Autor:
Malou Friederich-Persson, Fredrik Palm, Masaomi Nangaku, Erik Thörn, Max Levin, Peter Hansell
Publikováno v:
Hypertension. 62:914-919
Diabetic nephropathy is strongly associated with both increased oxidative stress and kidney tissue hypoxia. The increased oxidative stress causes increased kidney oxygen consumption resulting in kidney tissue hypoxia. To date, it has been difficult t
Autor:
S.-B. Catrina, Peter Hansell, Fredrik Palm, Gustav Dallner, Kerstin Brismar, Stephanie Franzén, M. Friederich Persson
Publikováno v:
Diabetologia. 55:1535-1543
Increased oxygen consumption results in kidney tissue hypoxia, which is proposed to contribute to the development of diabetic nephropathy. Oxidative stress causes increased oxygen consumption in type 1 diabetic kidneys, partly mediated by uncoupling
Publikováno v:
Acta Physiologica. 223:e13058
Aim Uncoupling protein-2 (UCP-2) can induce mitochondrial uncoupling in the diabetic kidney. Although mitochondrial uncoupling reduces oxidative stress originating from the mitochondria and can be regarded as a protective mechanism, the increased oxy
Autor:
Malou Friederich-Persson, Peter Hansell, Angelica Fasching, Patrik Persson, Fredrik Palm, Reiko Inagi
Publikováno v:
Acta physiologica (Oxford, England). 214(3)
Aim Diabetic patients are at increased risk for kidney disease. There is presently no clinical treatment available that effectively protects kidney function in diabetics. This study investigates whether chronic stimulation of the adenosine A2a recept
Autor:
Angelica Fasching, Malou Friederich-Persson, Masaomi Nangaku, Peter Hansell, Lina Nordquist, Per Liss, Fredrik Palm, Kumi Shoji
Publikováno v:
Journal of the American Society of Nephrology : JASN. 26(2)
Hyperglycemia results in increased oxygen consumption and decreased oxygen tension in the kidney. We tested the hypothesis that activation of hypoxia-inducible factors (HIFs) protects against diabetes-induced alterations in oxygen metabolism and kidn
Publikováno v:
Diabetes/Metabolism Research and Reviews. 20:452-459
Diabetes-induced renal complications, i.e. diabetes nephropathy, are a major cause of morbidity and mortality. The exact mechanism mediating the negative influence of hyperglycaemia on renal function is unclear, although several hypotheses have been
Autor:
Malou Friederich-Persson, Peter Hansell, Patrik Persson, Lina Nordquist, Angelica Fasching, Fredrik Palm
Publikováno v:
Oxygen Transport to Tissue XXXV ISBN: 9781461472568
Intrarenal tissue hypoxia is an acknowledged common pathway to end-stage renal disease in clinically common conditions associated with development of chronic kidney disease, such as diabetes and hypertension. In diabetic kidneys, increased oxygen met
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::c0e1cc9e569cc445a463c43d359970ea
https://doi.org/10.1007/978-1-4614-7411-1_2
https://doi.org/10.1007/978-1-4614-7411-1_2
Publikováno v:
Advances in Experimental Medicine and Biology ISBN: 9781461447719
Sustained hyperglycemia is closely associated with increased risk to develop nephropathy. We have previously reported alterations in the intrarenal oxygen metabolism already after the early onset of diabetes. Furthermore, formation of advanced glycat
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::0a08b4be581d92670b81bd06cbbca310
https://doi.org/10.1007/978-1-4614-4989-8_26
https://doi.org/10.1007/978-1-4614-4989-8_26